Oxidative Stress in Sepsis: A Focus on Cardiac Pathology.
Giuseppe BertozziMichela FerraraAldo Di FazioAniello MaieseGiuseppe DeloguNicola Di FazioVittoria TortorellaRaffaele La RussaVittorio FineschiPublished in: International journal of molecular sciences (2024)
This study aims to analyze post-mortem human cardiac specimens, to verify and evaluate the existence or extent of oxidative stress in subjects whose cause of death has been traced to sepsis, through immunohistological oxidative/nitrosative stress markers. Indeed, in the present study, i-NOS, NOX2, and nitrotyrosine markers were higher expressed in the septic death group when compared to the control group, associated with also a significant increase in 8-OHdG, highlighting the pivotal role of oxidative stress in septic etiopathogenesis. In particular, 70% of cardiomyocyte nuclei from septic death specimens showed positivity for 8-OHdG. Furthermore, intense and massive NOX2-positive myocyte immunoreaction was noticed in the septic group, as nitrotyrosine immunostaining intense reaction was found in the cardiac cells. These results demonstrated a correlation between oxidative and nitrosative stress imbalance and the pathophysiology of cardiac dysfunction documented in cases of sepsis. Therefore, subsequent studies will focus on the expression of oxidative stress markers in other organs and tissues, as well as on the involvement of the intracellular pattern of apoptosis, to better clarify the complex pathogenesis of multi-organ failure, leading to support the rationale for including therapies targeting redox abnormalities in the management of septic patients.
Keyphrases
- oxidative stress
- acute kidney injury
- induced apoptosis
- left ventricular
- dna damage
- diabetic rats
- ischemia reperfusion injury
- endoplasmic reticulum stress
- intensive care unit
- septic shock
- endothelial cells
- cell cycle arrest
- newly diagnosed
- heart failure
- reactive oxygen species
- gene expression
- cell death
- end stage renal disease
- poor prognosis
- cell proliferation
- nitric oxide
- atrial fibrillation
- angiotensin ii
- heat shock
- pi k akt